Streptococcus anginosus in the development and treatment of precancerous lesions of gastric cancer.

Abstract

The microbiota is strongly association with cancer. Studies have shown significant differences in the gastric microbiota between patients with gastric cancer (GC) patients and noncancer patients, suggesting that the microbiota may play a role in the development of GC. Although Helicobacter pylori (H. pylori) infection is widely recognized as a primary risk factor for GC, recent studies based on microbiota sequencing technology have revealed that non-H. pylori microbes also have a significant impact on GC. A recent study discovered that Streptococcus anginosus (S. anginosus) is more prevalent in the gastric mucosa of patients with GC than in that of those without GC. S. anginosus infection can spontaneously induce chronic gastritis, mural cell atrophy, mucoid chemotaxis, and heterotrophic hyperplasia, which promote the development of precancerous lesions of GC (PLGC). S. anginosus also disrupts the gastric barrier function, promotes the proliferation of GC cells, and inhibits apoptosis. However, S. anginosus is underrepresented in the literature. Recent reports suggest that it may cause precancerous lesions, indicating its emerging pathogenicity. Modern novel molecular diagnostic techniques, such as polymerase chain reaction, genetic testing, and Ultrasensitive Chromosomal Aneuploidy Detection, can be used to gastric precancerous lesions via microbial markers. Therefore, we present a concise summary of the relationship between S. anginosus and PLGC. Our aim was to further investigate new methods of preventing and treating PLGC by exploring the pathogenicity of S. anginosus on PLGC.